Inhibitor of DNA Binding 1, Dominant Negative Helix-Loop-Helix Protein (ID1) Kits ELISA

Zebrafish Inhibitor of DNA Binding 1, Dominant Negative Helix-Loop-Helix Protein (ID1) interaction partners

1. Gain and loss of id1 function in vivo demonstrated that Id1 promotes stem cell quiescence. The increased id1 expression observed in neural stem cells in response to injury appeared independent of inflammatory signals.

Mouse (Murine) Inhibitor of DNA Binding 1, Dominant Negative Helix-Loop-Helix Protein (ID1) interaction partners

1. The Id1(-/-) HSCs display a blunted proliferative response to such cytokines and other inducers of chronic proliferation including genotoxic and inflammatory stress and aging, protecting them from chronic stress and exhaustion.

2. study shows a biomechanical role of Id1 in endothelial cells' uptake of lipid by down-regulating LDLR, which could help understand how oscillatory flow affects atherosclerotic development.

3. We show that expression of Id-1, a negative regulator of myogenesis, is enhanced in Dnmt1-deficient cultures, leading to enhanced transdifferentiation of myoblasts toward the osteogenic lineage. Thus, these studies demonstrate that Dnmt1 influences cellular identity and determines lineage fidelity.

4. a loss of CULLIN3 represents a common signaling node for controlling the activity of intracellular WNT and SHH signaling pathways mediated by ID1

5. These results reveal a E2F1/miR-17-92/ENH1/Id1 regulatory axis during myogenesis.

6. Id1 enables both Lewis lung carcinoma cells and the host microenvironment for an effective liver colonization.

7. adipose tissue-specific overexpression of Id1 causes age-associated and high-fat diet-induced obesity in mice. Id1 suppresses BAT thermogenesis by binding to and suppressing PGC1alpha transcriptional activity. Lack of Id1 increases beige gene and Ucp1 expression in the WAT in response to cold exposure. Furthermore, brown-like differentiation is increased in Id1-deficient mouse embryonic fibroblasts.

8. If Gfi1 levels fall below a threshold, Id1 expression increases and renders E2A unable to function, which prevents hematopoietic progenitors from engaging along the B lymphoid lineage

9. Id1 may promote cell cycle progression of endothelial progenitor cells (EPCs), and that Wnt2 may be important in Id1 regulation of the cell cycle of EPCs.

10. Differential role of Id1 in MLL-AF9-driven leukemia based on cell of origin

11. Collectively, our results suggest that ENH1 plays an important role in the activation of myogenesis through the repression of Id2 activity.

12. Data indicate that upregulation of E2-2 protein markedly attenuated the inhibitor of DNA-binding 1 (ID1)-mediated increase in endothelial progenitor cells (EPCs) proliferation and migration.

13. these findings demonstrate that loss of Id compensation leads to dysregulation of the hematopoietic transcriptional network and multiple defects in erythropoietic development in adult mice.

14. our results strongly suggest that Usp1 is involved in the regulation of centrosome duplication, at least in part via ID1, and Usp1 may exert its oncogenic activity, partially through inducing centrosome abnormality.

15. demonstrated that Id1 and E2-2 are critical regulators of EPCs function in vitro. Id1 interacts with E2-2 and relieves the E2-2-mediated repression of FGFR1 and VEGFR2 expression to modulate EPCs functions

16. Endothelial ID1 up-regulation in inflamed colonic mucosa is an adaptive response that modulates the severity of tissue injury.

17. these findings provide in vivo genetic evidence of Id1 functions as an oncogene in breast cancer

18. overexpression leads to systemic immunosuppression by downregulation of key molecules involved in dendritic cell differentiation and suppression of CD8 T-cell proliferation, thus promoting primary tumour growth and metastatic progression

19. ID1/3 are crucial regulators of the adaptive antioxidant-mitochondrial response that promotes beta cell survival during oxidative stress through a novel link to the NFE2L2-small MAF pathway.

20. Using genetically modified mice, we found that loss of Id1 inhibited t(8;21) leukemia initiation and progression in vivo by abrogating protein kinase B (AKT)1 activation, and that Id1 interacted with AKT1 through its C terminus.

Human Inhibitor of DNA Binding 1, Dominant Negative Helix-Loop-Helix Protein (ID1) interaction partners

1. miR-338-5p can modulate 5-FU chemoresistance and inhibit invasion-related functions in ESCC by negatively regulating Id-1.

2. Findings highlight the prognostic significance of the transcriptional regulator Id1 in KRAS-mutant lung adenocarcinoma and provide mechanistic insight into how it controls tumor growth and metastasis.

3. ZEB1-AS1 can promote cell proliferation and migration of non-small cell lung carcinoma cells by silencing ID1 expression.

4. In acquired sorafenib-resistant cells, ID1 low expression, p16/IL6 axis up-regulation, and AKT phosphorylation activation were observed.

5. The miR-371 approximately 373/TGFBR2/ID1 signaling axis as a novel regulatory mechanism of TIC self-renewal.

6. Id-1 significantly promotes the proliferation and migration of human colon carcinoma cell lines SW480 and HT-29.

7. our results suggested that ID1 simultaneously regulates stemness through WNT and SHH signaling and differentiation through BMPR-mediated differentiation signaling in GSCs, informing a novel therapeutic strategy of combinatorial targeting of stemness and differentiation.

8. Knockdown of ID-1 suppressed proliferation and promoted apoptosis in hemangioma-derived endothelial cells.

9. study shows a biomechanical role of Id1 in endothelial cells' uptake of lipid by down-regulating LDLR, which could help understand how oscillatory flow affects atherosclerotic development.

10. ID1 overexpression is associated with histological subtype, lymph node metastasis, and unfavorable cancerspecific survival in penile squamous cell carcinoma.

11. Low ID1 expression is associated with breast cancer.

12. ID1, CTCF and ELK1 may be associated with prostate cancer, and may be potential therapeutic targets for the treatment of this disease.

13. CaMKII can directly phosphorylate Beclin 1 at Ser90 to promote K63-linked ubiquitination of Beclin 1 and activation of autophagy; it also promotes K63-linked ubiquitination of inhibitor of differentiation 1/2 (Id-1/2) by catalyzing phosphorylation of Id proteins and recruiting TRAF-6

14. ID1 expression was associated with the proliferation, invasion and migration of SACC cells. The observed inhibition of SACC cell growth, invasion and migration following knockdown of ID1 expression in the present study, may have been due to restoration of the balance between oncogenic and tumor-suppressive effects resulting from changes in the expression of downstream genes or associated proteins.

15. The mutual correlation between the expression level of TWIST1 and ID1 might be a critical factor driving the process of the human odontoblasts' differentiation.

16. a loss of CULLIN3 represents a common signaling node for controlling the activity of intracellular WNT and SHH signaling pathways mediated by ID1

17. Id1 enables lung cancer liver colonization by activating an epithelial mesenchymal transformation program in tumor cells and establishing the pre-metastatic niche.

18. High ID1 expression is associated with breast cancer.

19. ID1 expression impacts the sensitivity of colon cancer cells to 5-FU and may be considered as a potential predictive marker in colorectal carcinoma treatment.

20. Reducing ID1 gene expression reduces metastatic spread of salivary gland neoplasms.